Background: Sepsis is a state of disrupted inflammatory homeostasis that is often initiated by infection with a mortality ranging from 28-47%. The development and progression of sepsis are multi-factorial and affects the cardiovascular, immunological and endocrine systems of the body. Although recombinant atherogenic antigen (AHC) containing epitopes derived from ApoB, heat shock protein (HSP) 60, and Chlamydia pneumoniae outer membrane protein would represent the most successful vaccine candidate to reduce autoantigen (such as ApoB and HSP)-associated inflammation towards atherosclerosis, little is known about the potential effect of the immune response induced by AHC construct containing autoantigen epitopes on sepsis.

Aims: To assess whether immunization of C57BL/6 mice with the recombinant atherosclerotic antigen AHC has an effect on the outcome of induced sepsis.

Methods: 6-week old C57BL/6 mice (N=6 per group) were immunized with AHC and a non-immunized group served as control. Two weeks after the first immunization, the mice were subjected to cecal ligation and puncture (CLP) surgery to induce sepsis. Blood samples were collected at 6, 24, 48 and 72 h post CLP. Blood was taken at each time point and the level of plasma cytokines was measured by ELISA.

Results: Similar plasma levels of proinflammatory cytokines (IL-6 and TNF-alpha) and anti-inflammatory cytokine (IL-10) were observed in both AHC-immunized mice and non-immunized controls. Interestingly, the AHC-immunized mice showed better survival rate than non-immunized mice (5% versus 30%).

Conclusions: Immune response to AHC did not contribute to promotion of sepsis-induced inflammation in tested mice, indicating that CLP-induced inflammation may involve a different signal pathway from that of autoantigen (such as ApoB and HSP)-induced inflammation.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/immunization-with-recombinant-atherogenic-antigen-ahc-does-not-enhance-susceptibility-to-sepsis/